Experimental amniotic fluid embolism in animals produces profound pulmonary hypertension and acute cor pulmonale without evidence of left ventricular compromise. Authors reporting hemodynamic alterations associated with clinical amniotic fluid embolism have traditionally attempted to explain their findings within this experimental framework. A reanalysis of the five published cases of amniotic fluid embolism, which include hemodynamic data derived from pulmonary artery catheterization as well as a report of a sixth case suggests a hemodynamic interpretation different from the traditional one based on the animal model. Left ventricular failure is the only hemodynamic abnormality consistently observed in humans, and the published data are most readily explained on this basis alone. A theoretical model of hemodynamic changes accompanying amniotic fluid embolism that incorporates both experimental and clinical observations is presented. Therapeutic implications are discussed.